Kruppel-Like Factor 4 (KLF4) and its Regulation on Mitochondrial Homeostasis.

Journal of stem cell research & therapy Pub Date : 2018-01-01 Epub Date: 2018-09-14 DOI:10.4172/2157-7633.1000436
Brian Tung, Shuli Xia
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引用次数: 6

Abstract

Mitochondria are vital organelles that supply ATP and other energy metabolites to meet the bioenergetics demands of the cell. In environments of stress or increased energy requirement, mitochondria are highly dynamic and can undergo biogenesis, fusion/fission, or autophagy. The transcription factor family, Kruppel-Like Factor (KLF), is necessary to carry out normal cellular processes from proliferation to differentiation. Recently, its importance in metabolic homeostasis in various tissue types has gained much attention. A handful of evidence supports KLF4's involvement in regulating mitochondrial homeostasis in both healthy and cancer cells. In this review, we aim to summarize the available literature that demonstrates KLF4's ability to modulate the mitochondrial life cycle in: Cardiac tissue, in which KLF4-knockdown subsequently leads to Heart Failure (HF), andGlioblastoma (GBM), where its expression promotes extensive mitochondrial fusion and offers mild cell protection under serum-deprivation.

Abstract Image

Kruppel-Like Factor 4 (KLF4)及其对线粒体稳态的调控。
线粒体是提供ATP和其他能量代谢物以满足细胞生物能量需求的重要细胞器。在应激或能量需求增加的环境中,线粒体是高度动态的,可以发生生物发生、融合/裂变或自噬。转录因子家族,Kruppel-Like factor (KLF),是完成细胞从增殖到分化的正常过程所必需的。近年来,它在各种组织代谢稳态中的重要性已引起人们的广泛关注。少数证据支持KLF4参与调节健康细胞和癌细胞的线粒体稳态。在这篇综述中,我们旨在总结现有的文献,证明KLF4在心脏组织中调节线粒体生命周期的能力,在心脏组织中,KLF4敲低随后导致心力衰竭(HF),以及胶质母细胞瘤(GBM),其表达促进广泛的线粒体融合,并在血清剥夺下提供轻微的细胞保护。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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